Cancer cells rely primarily on glycolysis to generate cellular energy and biochemical intermediates for biosynthesis of lipids and nucleotides, while the majority of “normal” cells in adult tissues utilize aerobic respiration. This fundamental difference in cellular metabolism between cancer cells and normal cells is termed the Warburg Effect. As a result of this difference, pyruvate generated via the glycolytic pathway is converted to lactic acid, rather than being used to acetyl-CoA and eventually, the citrate utilized in a normal citric acid cycle. To compensate for these energetic changes and to maintain a citric acid cycle, cancer cells rely on glutamine metabolism which is achieved through, for an example, an elevation of glutaminase activity. Exploitation of this phenomenon can be achieved by inhibition of glutamine utilizing enzymes, for example, the elevated glutaminase activity. Phosphate-activated renal glutaminase (GLS1/KGA) has been shown to promote cancer cell proliferation at least in part via anaplerosis of the tricarboxylic acid cycle (TCA). GLS1 is not frequently mutated or amplified in tumors, making the selection of patients for treatment with a GLS inhibitor difficult. Therefore methods are needed to evaluate and/or select patients for treatment with GLS inhibitors.